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Published ahead of print on December 23, 2004, doi:10.1164/rccm.200404-532OC
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American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 579-586, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200404-532OC

Original Article

Effects of Allergen Challenge on Airway Epithelial Cell Gene Expression

Craig M. Lilly, Hiroki Tateno, Tsuyoshi Oguma, Elliot Israel and Larry A. Sonna

Combined Program in Pulmonary and Critical Care Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston; Thermal and Mountain Medicine Division, U.S. Army Research Institute of Environmental Medicine, Natick, Massachusetts; and Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, Tokyo, Japan

Correspondence and requests for reprints should be addressed to Craig M. Lilly, M.D., Pulmonary and Critical Care Division, Brigham and Women's Hospital, 75 Francis Street, Thorn 826C, Boston, MA 02115. E-mail: clilly{at}partners.org

Allergen exposure induces the airway epithelium to produce chemoattractants, proallergic interleukins, matrix-modifying proteins, and proteins that influence the growth and activation state of airway structural cells. These proteins, in turn, contribute to the influx of inflammatory cells and changes in structure that characterize the asthmatic airway. To use the response of the airway epithelium to allergen to identify genes not previously associated with allergic responses, we compared gene expression in cytokeratin-positive cells before and after segmental allergen challenge. After challenge with concentrations of allergen in the clinically relevant range, 755 (6%) of the detectable sequences had geometric mean fold-changes in expression, with 95% confidence intervals that excluded unity. Using a prospectively defined conservative filtering algorithm, we identified 141 sequences as upregulated and eight as downregulated, with confirmation by conventional polymerase chain reaction in all 10 sequences studied. Using this approach, we identified asthma-associated sequences including interleukin (IL-)-3, IL-4, and IL-5 receptor subunits, the p65 component of nuclear factor-{kappa}B, and lipocortin. The genomic response of the human airway to concentrations of allergen in the clinically relevant range involves a greater number of genes than previously recognized, including many not previously associated with asthma that are differentially expressed after airway allergen exposure.

Key Words: asthma • genomics • lung disease • segmental allergen challenge




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